When Salmonella typhimurium and Clostridium perfringens were tested in conventional chickens, larger numbers of S typhimurium and C perfringens adhered to Eimeria tenella-infected ceca than to uninfected ceca. In germ-free chickens, S typhimurium and C perfringens adhered to the E tenella-infected cecal mucosa more than to the uninfected cecal mucosa, but fewer Bacteroides vulgatus and Bifidobacterium thermophilum adhered to the E tenella-infected ceca than to the uninfected ceca. Many bacteria adhered to the lesions caused by E tenella as observed by scanning electron microscopy. On the basis of our findings, we suggest that infection with E tenella upsets the balance of competitive adherence of bacteria, allowing more colonization of S typhimurium and C perfringens.

Disposition kinetics of indocyanine green (ICG) were used to evaluate hepatic function in healthy Beagles (group 1; n = 6) and Beagles with progressive hepatic disease induced by oral administration of dimethylnitrosamine, a hepatospecific toxin. Three classes of hepatic disease were defined by histologic features: mild (group 2; n = 5), moderate (group 3; n = 6), and severe (group 4; n = 5). Disposition of ICG was studied 3 weeks following the last dose of toxin. A rapid IV injection of 0.5 mg of ICG/kg was administered and serum samples were obtained at certain intervals during 60-minute periods. Serum ICG was analyzed by use of visible spectrophotometry. Disposition kinetics were determined from serum ICG concentrations vs 15- and 60-minute time curves and compared between one another and among groups. Data based on 60-minute time curves were not significantly different from those based on 15-minute curves. Area under the curve for ICG was greatest in group 3. Clearance of ICG was decreased and mean resident time was increased in groups 3 and 4, compared with those in groups 1 and 2. When disposition data (60 minutes) were normalized for differences in hepatic weight among dogs, group-3 mean resident time was significantly greater than that of group 4. This study supports the diagnostic benefits of using ICG disposition kinetics as a method of evaluating hepatic function in dogs with progressive liver disease.

Pigs [9+/-1] weeks old) were inoculated with Streptococcus suis type 2, pseudorabies virus (PRV) or both. For each pig of groups A, B, and C the inoculum of S suis was 10(9) colony-forming units. For each pig of groups A, B, and D the inoculum of PRV was 5 X 10(3) TCID50 of either PRV strain 4892 (group A, n = 9) or PRV isolate B (group B, n = 9). The PRV strain 4892 is a highly virulent strain; isolate B causes mild clinical signs of infection in inoculated pigs. Group-C pigs (n = 9) were given S suis alone, and group-D pigs (n = 3) were inoculated only with PRV isolate B. Clinical signs of infection and development of lesions were readily seen in pigs of groups A, B, and C. Duration and severity of clinical signs of disease and lesions were reduced in pigs of group C, compared with those of the other 2 groups. Lesions, such as polyarthritis and fibrinous pericarditis, were more abundant and acute in the groups of pigs given mixed challenge exposure, compared with pigs inoculated exclusively with S suis type 2 (group C). The group of pigs inoculated with PRV isolate B alone did not manifest clinical signs of disease or lesions. Average daily gain for group-C pigs was higher, compared with that of other groups; the difference was statistically significant at P < 0.02 and P < 0.05 for groups B and D, respectively. Spread of S suis within the tissues of infected pigs was higher in pigs of groups A and B, compared with pigs of group C. Total number of isolations was 8, 15, and 7 for groups A, B, and C, respectively; S suis was isolated from more than 1 tissue specimen from some pigs. The rate of pigs carrying S suis was 4 of 4 in group-A, 7 of 9 in group-B, and 5 of 9 in group-C pigs. It was concluded that clinical disease associated with S suis type 2 was enhanced by concomitant infection with PRV and such effect was common to both PRV strains tested, the highly virulent strain and the strain with low virulence.

Lymphoscintigraphic evaluation of the thoracic duct (TD) was performed in 10 healthy and 12 dogs with experimentally created TD abnormalities (6 dogs with TD lacerations and 6 dogs with cranial vena ligations). Complete imaging took 4 hours and caused no adverse effects or complications. Lymphoscintigraphy of healthy dogs failed to image the TD; however, background activity in the abdomen and thorax, and radioactivity in the kidneys, bladder, liver, and heart were noticed. Lacerations and transections of the TD were experimentally created, in 6 dogs to ascertain whether TD rupture could be detected with lymphoscintigraphy. Lymphoscintigraphy was performed within 48 hours of creating the TD defect. There was no significant difference in the scintigraphic pattern of healthy dogs and those with experimentally created TD defects. Ligation of the cranial vena cava was performed in 6 dogs; 3 dogs developed chylothorax. In those 3 dogs, diffuse radioactivity was imaged in the thorax and was compatible with thoracic lymphangiectasia. In one of these dogs, linear activity consistent with the TD and localized regions of radioactivity cranial to the heart (compatible with the mediastina lymph nodes) were noticed. Lymphoscintigraphic findings in these dogs correlated with lymphangiographic findings.

The effects of 3 experimental diets that varied only in the source of dietary protein (ie, poultry, cereal, red meat) were compared in Basenjis (n = 8) with immunoproliferative enteropathy and healthy Beagles (n = 8). Significant differences in fecal character, serum IgA concentration, and intestinal digestive and absorptive function were not induced by the different sources of dietary protein. The results of this study do not support a causal role for dietary protein source in the pathogenesis of immunoproliferative enteropathy of Basenjis.

The lungs of sensitized horses were exposed to aerosolized ovalbumin. Some horses (n = 4) were given ovalbumin in 1 lung only, whereas in others (n = 7), ovalbumin or vehicle were inoculated in the cranial, ventral, and caudal regions of the caudal lung lobe. Horses were exercised 5 hours after ovalbumin exposure. Immediately before exercise, endoscopy failed to reveal any abnormality. After exercise, endoscopic examination of horses subjected to unilateral ovalbumin exposure revealed extensive blood in airways leading to the exposed lung in all horses. Blood was not observed in the airways leading to the control lung. Mean (+/- SEM) minimum volume of the exposed and control lungs was 9.5 +/- 1.5 and 5.5 +/- 1.6 L, respectively; this difference was statistically significant (P < 0.05). Bronchoscopy of horses subjected to regional ovalbumin or vehicle exposure and exercise revealed a small amount of blood-tinged fluid in the bronchi serving the regions of the lung inoculated with ovalbumin. Minimum volumes of such regions were not significantly different from one another. However, their minimum volume was significantly (P < 0.05) larger than that of vehicle-inoculated regions. Gross and histologic examination confirmed inflammation and hemorrhage in the ovalbumin-exposed, but not the control lungs or lung regions. Thus, exercise can cause blood from an injured region of lung to appear in the larger airways. Regional differences in lung structure and function do not influence the appearance of blood in the airways.